Apo B versus cholesterol in estimating cardiovascular risk and in guiding therapy: report of the thirty‐person/ten‐country panel

Philip J. Barter(The Heart Research Institute), Christie M. Ballantyne(Baylor College of Medicine), Rafael Carmena(Hospital Clínico Universitario de Valencia), Manuel Castro Cabezas(Sint Franciscus Gasthuis), M. John Chapman(Sorbonne Université), Patrick Couture(Centre hospitalier universitaire de Québec), Jacqueline de Graaf(Radboud University Nijmegen), Paul N. Durrington(Manchester Royal Infirmary), Ole Færgeman(Aarhus University Hospital), J. Fröhlich(University of British Columbia), Curt D. Furberg(The Heart Research Institute), C Gagné(Baylor College of Medicine), Steven M. Haffner(The University of Texas at San Antonio Health Science Center), Steve E. Humphries(The Royal Free Hospital), Ingmar Jungner(Karolinska Institutet), Ronald M. Krauss, Peter O. Kwiterovich, S Marcovina(University of Washington), Chris J. Packard(Glasgow Royal Infirmary), Thomas A. Pearson(University of Rochester), K. Srinath Reddy(All India Institute of Medical Sciences), Robert S. Rosenson(Northwestern University), Nizal Sarrafzadegan, Allan D. Sniderman(McGill University Health Centre), Anton F. H. Stalenhoef(Radboud University Nijmegen), Evan A. Stein(Baylor College of Medicine), Philippa J. Talmud(The Royal Free Hospital), Andrew Tonkin(Radboud University Nijmegen), Göran Walldius(Karolinska Institutet), K. Williams(The University of Texas at San Antonio Health Science Center)
Journal of Internal Medicine
February 10, 2006
Cited by 471Open Access
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Abstract

There is abundant evidence that the risk of atherosclerotic vascular disease is directly related to plasma cholesterol levels. Accordingly, all of the national and transnational screening and therapeutic guidelines are based on total or LDL cholesterol. This presumes that cholesterol is the most important lipoprotein-related proatherogenic risk variable. On the contrary, risk appears to be more directly related to the number of circulating atherogenic particles that contact and enter the arterial wall than to the measured concentration of cholesterol in these lipoprotein fractions. Each of the atherogenic lipoprotein particles contains a single molecule of apolipoprotein (apo) B and therefore the concentration of apo B provides a direct measure of the number of circulating atherogenic lipoproteins. Evidence from fundamental, epidemiological and clinical trial studies indicates that apo B is superior to any of the cholesterol indices to recognize those at increased risk of vascular disease and to judge the adequacy of lipid-lowering therapy. On the basis of this evidence, we believe that apo B should be included in all guidelines as an indicator of cardiovascular risk. In addition, the present target adopted by the Canadian guideline groups of an apo B <90 mg dL(-1) in high-risk patients should be reassessed in the light of the new clinical trial results and a new ultra-low target of <80 mg dL(-1) be considered. The evidence also indicates that the apo B/apo A-I ratio is superior to any of the conventional cholesterol ratios in patients without symptomatic vascular disease or diabetes to evaluate the lipoprotein-related risk of vascular disease.


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